Evidence map›Paper›PMID 36528068›Full record

ReviewBiochemical pharmacology2023

Functions of the aryl hydrocarbon receptor (AHR) beyond the canonical AHR/ARNT signaling pathway.

Natalie C Sondermann, Sonja Faßbender, Frederick Hartung, Anna M Hätälä, Katharina M Rolfes, Christoph F A Vogel, Thomas Haarmann-Stemmann

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 2 pooled it
10.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
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  8. AhR activation inhibits DRP1-induced mitochondrial fission in airway smooth muscle during asthma.American journal of respiratory cell and molecular biology · 2026
    Article
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44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Natalie C SondermannIUF - Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Sonja FaßbenderIUF - Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Frederick HartungIUF - Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Anna M HätäläIUF - Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Katharina M RolfesIUF - Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Christoph F A VogelDepartment of Environmental Toxicology and Center for Health and the Environment, University of California, Davis, CA 95616, USA.
Thomas Haarmann-StemmannIUF - Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany. Electronic address: thomas.haarmann-stemmann@iuf-duesseldorf.de.
Leibniz Institute of Environmental Medicine · DEUniversity of California, Davis · US

Funding

UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Irva Hertz-Picciotto · 2015 to 2026
$26.0M
Air pollution, atherosclerosis, and the role of the aryl hydrocarbon receptorR01ES029126 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2019 to 2023
$1.8M
The impact of Aryl hydrocarbon receptor signaling on Toll like receptor-mediated inflammationR01ES032827 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHRISTOPH F A VOGEL · 2022 to 2026
$1.7M
NIEHS NIH HHS P30 ES023513NIEHS NIH HHS R01 ES029126NIEHS NIH HHS R01 ES032827
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-dependent transcription factor regulating adaptive and maladaptive responses toward exogenous and endogenous signals. Research from various biomedical disciplines has provided compelling evidence that the AHR is critically involved in the pathogenesis of a variety of diseases and disorders, including autoimmunity, inflammatory diseases, endocrine disruption, premature aging and cancer. Accordingly, AHR is considered an attractive target for the development of novel preventive and therapeutic measures. However, the ligand-based targeting of AHR is considerably complicated by the fact that the receptor does not always follow the beaten track, i.e. the canonical AHR/ARNT signaling pathway. Instead, AHR might team up with other transcription factors and signaling molecules to shape gene expression patterns and associated physiological or pathophysiological functions in a ligand-, cell- and micromilieu-dependent manner. Herein, we provide an overview about some of the most important non-canonical functions of AHR, including crosstalk with major signaling pathways involved in controlling cell fate and function, immune responses, adaptation to low oxygen levels and oxidative stress, ubiquitination and proteasomal degradation. Further research on these diverse and exciting yet often ambivalent facets of AHR biology is urgently needed in order to exploit the full potential of AHR modulation for disease prevention and treatment.

Indexed as

Aryl Hydrocarbon Receptor Nuclear TranslocatorReceptors, Aryl HydrocarbonBasic Helix-Loop-Helix ProteinsGene Expression RegulationHumansLigandsSignal TransductionAHR protein, humanARNT protein, humanAryl Hydrocarbon Receptor Nuclear TranslocatorBasic Helix-Loop-Helix ProteinsLigandsReceptors, Aryl HydrocarbonAryl hydrocarbon receptorImmune responseNon-canonical signalingSignal transductionTranscription factorUbiquitination

Identifiers

PMID36528068
PMCPMC9884176
OpenAlexW4313201375

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.